title: Pathophysiology and management of fluid and electrolyte disturbances in patients on chronic dialysis with severe hyperglycemia.
abstract: The mechanisms of fluid and solute abnormalities that should be considered in any patient with severe hyperglycemia include changes in the total amount of extracellular solute, osmotic diuresis, intake of water driven by thirst, and influences from associated conditions. The absence of osmotic diuresis distinguishes dialysis-associated hyperglycemia (DH) from hyperglycemia with preserved renal function (HPRF). Mainly because of this absence, comparable degrees of hyperglycemia tend to produce less hypertonicity and less severe intracellular volume contraction in DH than in HPRF, while extracellular volume is expanded in DH but contracted in HPRF. Ketoacidosis can develop in both DH and HPRF. Among DH patients, hyperkalemia appears to be more frequent when ketoacidosis is present than when nonketotic hyperglycemia is present. Among HPRF patients, the frequency of hyperkalemia appears to be similar whether ketoacidosis or nonketotic hyperglycemia is present. Usually patients with severe DH have no symptoms or may exhibit a thirst. Infrequent clinical manifestations of DH include coma and seizures from hypertonicity or ketoacidosis and pulmonary edema from extracellular expansion. Insulin infusion is usually the only treatment required to correct the biochemical abnormalities and reverse the clinical manifestations of DH. Monitoring of the clinical manifestations and biochemical parameters during treatment of DH with insulin is needed to determine whether additional measures, such as administration of saline, free water, or potassium salts, as well as emergency hemodialysis (HD) are needed. Emergency HD carries the risk of excessively rapid decline in tonicity; its benefits in the treatment of DH have not been established.
authors.affiliation: New Mexico Veterans Affairs Health Care System, Albuquerque, New Mexico 87108, USA. antonios.tzamaloukas@med.va.gov
authors.forename: Antonios H
authors.initials: AH
authors.lastname: Tzamaloukas
authors.forename: Todd S
authors.initials: TS
authors.lastname: Ing
authors.forename: Kostas C
authors.initials: KC
authors.lastname: Siamopoulos
authors.forename: Dominic S C
authors.initials: DS
authors.lastname: Raj
authors.forename: Moses S
authors.initials: MS
authors.lastname: Elisaf
authors.forename: Mark
authors.initials: M
authors.lastname: Rohrscheib
authors.forename: Glen H
authors.initials: GH
authors.lastname: Murata
mesh_terms: D000137:Acid-Base Imbalance / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy*; D001834:Body Water; D045604:Extracellular Fluid; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D007676:Kidney Failure, Chronic / Q000150:complications / Q000503:physiopathology / Q000628:therapy; D006435:Renal Dialysis / Q000009:adverse effects*; D014883:Water-Electrolyte Imbalance / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy*